Posts Tagged ‘obesity’


Ghrelin, the hormone that makes you hungry, also makes food, and food smells, irresistibly appealing. Karen Hopkin reports.

By Karen Hopkin

‘Tis the season…for overeating! But it’s not just your lack of willpower or the omnipresent holiday treats. No, you can lay some of the blame on ghrelin. Because a new study shows that ghrelin, the hormone that makes you hungry, also makes food…and food smells…irresistibly appealing. The finding appears in the journal Cell Reports. [Jung Eun Han et al, Ghrelin Enhances Food Odor Conditioning in Healthy Humans: An fMRI Study]

Ghrelin is produced in the stomach, and its levels rise before your habitual mealtimes and after you haven’t eaten for an extended period. So the hormone reminds you to put something in your belly. Injecting rats with ghrelin encourages them to eat…and people who receive a dose of ghrelin grab extra helpings from the buffet.

But how does the hormone induce overindulgence? To find out, researchers at McGill University trained volunteers to associate random images with the smell of food. For example, every time they saw a tree, they might get a whiff of freshly baked bread. At the same time, some of the subjects received ghrelin; others got only saline.

The volunteers were then ushered into an fMRI machine, where the researchers watched their brains to see which parts got turned on by different images.

Seems that in subjects under the influence of ghrelin, the brain region involved in pleasure and reward lit up only when volunteers viewed the images they associated with food aromas. Their brain pleasure centers were disinterested in images that had not been paired with food smells.

Also, when participants were then asked to rate the pleasantness of the images, the ones who’d been exposed to ghrelin gave higher grades to the food-associated pictures than did folks who got no ghrelin.

https://www.scientificamerican.com/podcast/episode/hunger-hormone-ghrelin-aids-overindulgence/

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Weight gain trajectories in early childhood are related to the composition of oral bacteria of two-year-old children, suggesting that this understudied aspect of a child’s microbiota — the collection of microorganisms, including beneficial bacteria, residing in the mouth — could serve as an early indicator for childhood obesity. A study describing the results appears September 19 in the journal Scientific Reports.

“One in three children in the United States is overweight or obese,” said Kateryna Makova, Pentz Professor of Biology and senior author of the paper. “If we can find early indicators of obesity in young children, we can help parents and physicians take preventive measures.”

The study is part of a larger project with researchers and clinicians at the Penn State Milton S. Hershey Medical Center called INSIGHT, led by Ian Paul, professor of pediatrics at the Medical Center, and Leann Birch, professor of foods and nutrition at the University of Georgia. The INSIGHT trial includes nearly 300 children and tests whether a responsive parenting intervention during a child’s early life can prevent the development of obesity. It is also designed to identify biological and social risk factors for obesity.

“In this study, we show that a child’s oral microbiota at two years of age is related to their weight gain over their first two years after birth,” said Makova.

The human digestive tract is filled with a diverse array of microorganisms, including beneficial bacteria, that help ensure proper digestion and support the immune system. This “microbiota” shifts as a person’s diet changes and can vary greatly among individuals. Variation in gut microbiota has been linked to obesity in some adults and adolescents, but the potential relationship between oral microbiota and weight gain in children had not been explored prior to this study.

“The oral microbiota is usually studied in relation to periodontal disease, and periodontal disease has in some cases been linked to obesity,” said Sarah Craig, a postdoctoral scholar in biology at Penn State and first author of the paper. “Here, we explored any potential direct associations between the oral microbiota and child weight gain. Rather than simply noting whether a child was overweight at the age of two, we used growth curves from their first two years after birth, which provides a more complete picture of how the child is growing. This approach is highly innovative for a study of this kind, and gives greater statistical power to detect relationships.”

Among 226 children from central Pennsylvania, the oral microbiota of those with rapid infant weight gain — a strong risk factor for childhood obesity — was less diverse, meaning it contained fewer groups of bacteria. These children also had a higher ratio of Firmicutes to Bacteroidetes, two of the most common bacteria groups found in the human microbiota.

“A healthy person usually has a lot of different bacteria within their gut microbiota,” said Craig. “This high diversity helps protect against inflammation or harmful bacteria and is important for the stability of digestion in the face of changes to diet or environment. There’s also a certain balance of these two common bacteria groups, Firmicutes and Bacteroidetes, that tends to work best under normal healthy conditions, and disruptions to that balance could lead to dysregulation in digestion.”

Lower diversity and higher Firmicutes to Bacteroidetes (F:B) ratio in gut microbiota are sometimes observed as a characteristic of adults and adolescents with obesity. However, the researchers did not see a relationship of weight gain with either of these measures in gut microbiota of two-year-olds, suggesting that the gut microbiota may not be completely established at two years of age and may still be undergoing many changes.

“There are usually dramatic changes to an individual’s microbiota as they develop during early childhood,” said Makova. “Our results suggest that signatures of obesity may be established earlier in oral microbiota than in gut microbiota. If we can confirm this in other groups of children outside of Pennsylvania, we may be able to develop a test of oral microbiota that could be used in clinical care to identify children who are at risk for developing obesity. This is particularly exciting because oral samples are easier to obtain than those from the gut, which require fecal samples.”

Interestingly, weight gain in children was also related to diversity of their mother’s oral microbiota. This could reflect a genetic predisposition of the mother and child to having a similar microbiota, or the mother and child having a similar diet and environment.

“It could be a simple explanation like a shared diet or genetics, but it might also be related to obesity,” said Makova. “We don’t know for sure yet, but if there is an oral microbiome signature linked to the dynamics of weight gain in early childhood, there is a particular urgency to understand it. Now we are using additional techniques to look at specific species of bacteria–rather than larger taxonomic groups of bacteria–in both the mothers and children to see whether specific bacteria species influence weight gain and the risk of obesity.”

In addition to Makova, Craig, Paul, and Birch, the research team includes Jennifer Savage, Michele Marini, Jennifer Stokes, Anton Nekrutenko, Matthew Reimherr, and Francesca Chiaromonte from Penn State, Daniel Blankenberg from the Cleveland Clinic, and Alice Carla Luisa Parodi from Politecnico di Milano. INSIGHT (Intervention Nurses Start Infants Growing on Healthy Trajectories) is coordinated through the Penn State Milton S. Hershey Medical Center.

This work is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); the Penn State Eberly College of Science; the Penn State Institute for Cyberscience; the National Center for Research Resources and the National Center for Advancing Translational Sciences of the National Institutes of Health (NIH); and the Pennsylvania Department of Health using Tobacco CURE funds.

http://science.psu.edu/news-and-events/2018-news/Makova9-2018

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Obesity leads to cognitive impairment by activating microglial cells, which consume otherwise functional synapses in the hippocampus, according to a study of male mice published in JNeurosci. The research suggests that microglia may be a potential therapeutic target for one of the lesser known effects of this global health epidemic on the brain.

Nearly two billion adults worldwide are overweight, more than 600 million of whom are obese. In addition to increasing risk of conditions such as diabetes and heart disease, obesity is also a known risk factor for cognitive disorders including Alzheimer’s disease. The cellular mechanisms that contribute to cognitive decline in obesity, however, are not well understood.

Elise Cope and colleagues replicated previous research by demonstrating diet-induced obesity in mice impairs performance on cognitive tasks dependent on the hippocampus and results in loss of dendritic spines — the neuronal protrusions that receive signals from other cells — and activates microglia. Using genetic and pharmacological approaches to block microglial activity, the researchers established microglia are causally linked to obesity-induced dendritic spine loss and cognitive decline. The results suggest obesity may drive microglia into a synapse-eating frenzy that contributes to the cognitive deficits observed in this condition.

https://www.technologynetworks.com/neuroscience/news/brains-immune-cells-to-blame-for-obesity-associated-cognitive-decline-309339?utm_campaign=NEWSLETTER_TN_Neuroscience_2017&utm_source=hs_email&utm_medium=email&utm_content=65859986&_hsenc=p2ANqtz-8GahP4LE2EOoHR4ShLvP0WjIDGrQksSkIDt93_VTrGea3qFC8v7VaOr9RXxmjjl8VDuNn2DK1PVOXEa5FBOdgl-GvhlA&_hsmi=65859986

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A UNSW-led team researching a drug to avoid insulin resistance was greeted with an unexpected result that could have implications for the nation’s rising rates of obesity and associated disease.

A novel drug is being touted as a major step forward in the battle against Australia’s escalating rates of obesity and associated metabolic diseases.

Two in three adults in Australia are overweight or obese. A long-term study between researchers at the Centenary Institute and UNSW Sydney has led to the creation of a drug which targets an enzyme linked to insulin resistance – a key contributor of metabolic diseases, such as type 2 diabetes.

The project has been a collaboration between the Centenary Institute’s Associate Professor Anthony Don, UNSW’s Metabolic research group and its leader Associate Professor Nigel Turner, and UNSW Professor Jonathan Morris’ synthetic chemistry group. Together, they set out to create a drug that targeted enzymes within the Ceramide Synthase family, which produce lipid molecules believed to promote insulin resistance in skeletal muscle, as well as liver and fat tissue.

The study has been published in the highly-regarded scientific journal Nature Communications. Surprisingly, although the drug was very effective at reducing the lipids of interest in skeletal muscle, it did not prevent mice (which had been fed a high-fat diet to induce metabolic disease) from developing insulin resistance. Instead, it prevented the mice from depositing and storing fat by increasing their ability to burn fat in skeletal muscle.

“We anticipated that targeting this enzyme would have insulin-sensitising, rather than anti-obesity, effects. However, since obesity is a strong risk factor for many different diseases including cardiovascular disease and cancer, any new therapy in this space could have widespread benefits,” says UNSW Associate Professor Nigel Turner.

While the study produced some unexpected results, it’s the first time scientists have been able to develop a drug that successfully targets a specific Ceramide Synthase enzyme in metabolic disease, making it a significant advancement in the understanding and prevention of a range of chronic health conditions.

“From here, I would like to develop drugs which target both the Ceramide Synthase 1 and 6 enzymes together, and see whether it produces a much stronger anti-obesity and insulin sensitising response. Although these drugs need more work before they are suitable for use in the clinic, our work so far has been a very important step in that direction,” says Centenary Institute’s Associate Professor Anthony Don.

https://newsroom.unsw.edu.au/news/health/surprise-result-researchers-targeting-high-rates-obesity


Adipose Connective Tissue Stores Fat in Our Body. Credit: Berkshire Community College Bioscience Image Library

A new technique to study fat stores in the body could aid efforts to find treatments to tackle obesity.

The approach focuses on energy-burning tissues found deep inside the body – called brown fat – that help to keep us warm when temperatures drop.

Experts are aiming to find it this calorie-burning power can be harnessed to stop weight gain, but little is known about how the process works.

Previous studies have mainly relied on a medical imaging technique called PET/CT to watch brown fat in action deep inside the body. But the method is unable to directly measure the chemical factors in the tissue.

Scientists at the University of Edinburgh developed a technique called microdialysis to measure how brown fat generates heat in people.

The approach involves inserting a small tube into an area of brown fat in the body and flushing it with fluid to collect a snapshot of the tissues’ chemical make-up.

The team tested the technique in six healthy volunteers, using PET/CT to guide the tube to the right location.

They discovered that in cold conditions, brown fat uses its own energy stores and other substances to generate heat.

Brown fat was active under warm conditions too, when the body does not need to generate its own heat, an outcome that had not been seen before.

Researchers hope the technique will help them to analyse the specific chemicals involved, so that they can better understand how brown fat works.

Most of the fat in our body is white fat, which is found under the skin and surrounding internal organs. It stores excess energy when we consume more calories than we burn.

Brown fat is mainly found in babies and helps them to stay warm. Levels can decrease with age but adults can still have substantial amounts of it, mainly in the neck and upper back region. People who are lean tend to have more brown fat.

The study, published in Cell Metabolism, was funded by the Medical Research Council and Wellcome.

Lead researcher Dr Roland Stimson, of the British Heart Foundation Centre for Cardiovascular Science at the University of Edinburgh, said: “Understanding how brown fat is activated could reveal potential targets for therapies that boost its energy-burning power, which could help with weight loss.”

This article has been republished from materials provided by the University of Edinburgh. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference: Weir, G., Ramage, L. E., Akyol, M., Rhodes, J. K., Kyle, C. J., Fletcher, A. M., … Stimson, R. H. (2018). Substantial Metabolic Activity of Human Brown Adipose Tissue during Warm Conditions and Cold-Induced Lipolysis of Local Triglycerides. Cell Metabolism, 0(0). https://doi.org/10.1016/j.cmet.2018.04.020

https://www.technologynetworks.com/proteomics/news/how-brown-fat-keeps-us-warm-304351?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=63228690&_hsenc=p2ANqtz-9oqDIw3te1NPoj51s94kxnA1ClK8Oiecfela6I4WiITEbm_-SWdmw6pjMTwm2YP24gqSzRaBvUK1kkb2kZEJKPcL5JtQ&_hsmi=63228690

In a new study researchers from the Institute for Experimental Pediatric Endocrinology of the Charité – Universitätsmedizin Berlin have successfully treat patients whose obesity is caused by a genetic defect. Aside from its beneficial effects on the patients, the researchers also provided insights into the fundamental signaling pathways regulating satiety of the new drug. The results of this research have been published in Nature Medicine*.

A mutation in the gene encoding the leptin receptor (LEPR) can cause extreme hunger starting with the first months of life. As a result, affected individuals develop extreme obesity during childhood. Increased exercise and reduced caloric intake are usually insufficient to stabilize body-weight. In many cases, obesity surgery fails to deliver any benefits, meaning that a drug-based treatment approach becomes increasingly important.

Two years ago, Dr. Peter Kühnen and the working group successfully demonstrated that treatment with a peptide, which activates the melanocortin 4 receptor (MC4R) could play a central role in the body’s energy metabolism and body weight regulation. Leptin, which is also known as the satiety (or starvation) hormone, normally binds to the LEPR, triggering a series of steps that leads to the production of melanocyte-stimulating hormone (MSH). The act of MSH by binding to its receptor, the melanocortin 4 receptor (MC4R) which transduce the satiety signal to the body. However, if the LEPR is defective, the signaling cascade is interrupted. The patient’s hunger remains unabated, placing them at greater risk of becoming obese. As part of this current study, researchers used a peptide that binds to the MC4R in the brain, and this activation trigger the normal satiety signal. Working in cooperation with the Clinical Research Unit at the Berlin Institute of Health (BIH), the researchers were able to record significant weight loss in patients with genetic defects affecting the LEPR.

“We also wanted to determine why the used peptide was so effective and why, in contrast to other preparations with a similar mode of action, it did not produce any severe side effects,” explains Dr. Kühnen. “We were able to demonstrate that this treatment leads to the activation of a specific and important signaling pathway, whose significance had previously been underestimated.” Dr. Kühnen’s team is planning to conduct further research to determine whether other patients might benefit from this drug: “It is possible that other groups of patients with dysfunctions affecting the same signaling pathway might be suitable candidates for this treatment.”

*Clément K, et al., MC4R agonism promotes durable weight loss in patients with leptin receptor deficiency, Nature Medicine (2018), doi:10.1038/s41591-018-0015-9.

https://www.charite.de/en/service/press_reports/artikel/detail/den_unstillbaren_hunger_abschalten/

Is your child having a tough time sleeping properly? You may need to keep a check on his/her body mass index (BMI) as a new research suggests that there is a co-relation between the two and can lead to cancer in adulthood.

“Childhood obesity very often leads to adult obesity. This puts them at greater risk of developing obesity-related cancers in adulthood,” said study lead author Bernard Fuemmeler, Professor and Associate Director for Cancer Prevention and Control at the Virginia Commonwealth University.

For the study, researchers enrolled 120 children, with an average age of eight, whose mothers had participated in the Newborn Epigenetic Study both pre-birth and during early childhood.

To track the sleep-wake cycle, the children wore accelerometers continuously for 24 hours a day for a period of at least five days.

They found that shorter sleep duration, measured in hours, was associated with a higher BMI z-score (body mass index adjusted for age and sex).

Each additional hour of sleep was associated with a .13 decrease in BMI z-score and with a 1.29 cm decrease in waist circumference.

More fragmented rest-activity rhythms and increased intradaily variability — a measure of the frequency and extent of transitions between sleep and activity — were also associated with greater waist circumferences.

The study results, to be presented at Obesity and Cancer: Mechanisms Underlying Etiology and Outcomes, indicate that while sleep duration is important, examining markers of sleep quality may also be useful in designing childhood obesity prevention strategies.

“Today, many children are not getting enough sleep. There are a number of distractions, such as screens in the bedroom, that contribute to interrupted, fragmented sleep. This, perpetuated over time, can be a risk factor for obesity,” Fuemmeler said.

“Because of the strong links between obesity and many types of cancer, childhood obesity prevention is cancer prevention.”

Proper sleep in children may prevent cancer later